Review Article

Nitric Oxide, Oxidative Stress, and Interplay in Diabetic Endothelial Dysfunction

Figure 3

role in intracellular ROS production.   modulates ROS production by using three mechanisms. The nuclear mechanism involves mediated FOXO transcription factors inhibition, leading to decreased expression of ROS-scavenging enzymes such as catalase (CAT) and manganese superoxide dismutase (MnSOD). At the plasma membrane, promotes RAC1 activation and triggers NADPH membrane oxidase-ROS production. acts in the mitochondrial intermembrane space (IMS). In response to oxidative stress, is serine phosphorylated by PKCβII and isomerized by the peptidylprolyl cis/trans isomerase PIN1. This isomerization allows the dephosphorylation of Ser-36 residue by the serine threonine phosphatase PP2A, inducing the translocation from the cytosol to the IMS. In the IMS, binds to cytochrome c (Cyt c), generating ROS. These ROS activate the release of mitochondrial apoptotic factors, eventually inducing apoptosis.
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